Use of means for trapping co2 in a filter for preventing inflammation, cancer and cardiovascular diseases in a subject exposed to tobacco smoke

ABSTRACT

The invention comprises the use of means for trapping CO 2  in a filter for preventing inflammation, cancer and/or cardiovascular diseases in a subject exposed to tobacco smoke.

The present invention relates to a filter composition comprising meansfor trapping CO₂ for preventing inflammation, cancer and/orcardiovascular diseases in a subject exposed to tobacco smoke.

It relates more particularly to a cigarette filter designed forselectively adsorbing CO₂ from the gases resulting from the burning oftobacco, inhaled by a smoker or by a subject exposed to tobacco smoke.

It is well known that smoking is the cause of a large number of cases oflung and throat cancers. In fact, the burning of tobacco in a cigarette,a cigar or a pipe gives rise to smoke that contains numerous chemicalsubstances originating from the tobacco leaf, or that form by chemicalreaction when tobacco is consumed. Some of these substances are classedas being carcinogenic or mutagenic, and in fact are involved in thedevelopment of tumours in the throat or in the lungs.

Moreover, the major role of tobacco in the incidence of myocardialinfarction and of coronary artery diseases has been known for many years[Ambrose J A et al., The pathophysiology of cigarette smoking andcardiovascular diseases: an update (2004) J Am Coll Cardiol. May 19;43(10):1731-7]. However, the action mechanisms involved in thesediseases are still largely unknown.

Tobacco smoke, in its main, primary stream, i.e. as inhaled directly bya smoker when the latter activates the combustion of tobacco, via acigarette or by means of a pipe, is an aerosol composed of a gas phaseand a particulate phase.

The particulate phase comprises particles with diameter between 0.1 and1 μm, which, owing to their small size, reach the pulmonary alveoli.These particles often contain toxic organic products which areprecipitated on contact with the alveolar membranes and form depositsthat are not easily eliminated by the body (tars) or which dissolve inthe cytoplasm of the cells, forming free radicals which react withvarious cellular constituents (mutagenic, cytotoxic etc.).

The most basic cigarette filters are generally constituted of a filtercomposition comprising entangled cellulose fibres, with the primary aimof retaining the fine particles.

The gas phase, constituted to 80% by nitrogen and oxygen from theatmospheric air, includes from 12 to 15% of carbon dioxide (CO₂), 3 to6% of carbon monoxide (CO), 0.1 to 0.2% of hydrogen cyanide (CHN) and 1to 3% of various volatile organic compounds and in particular nitrogenoxides (NOx) [Norman, V. An overview of the vapor phase, semi volatileand non volatile components of cigarette smoke (1997) Recent Advances inTobacco Science, 3:28-58].

The amounts of gas are expressed here as molar percentage relative tothe total gases constituting the gas phase. The nitrogen oxides formfree radicals that are very irritant and can notably cause asthmaattacks. Hydrogen cyanide and carbon monoxide display great affinity forerythrocytes, which transport the oxygen in the blood, and can causeanaemias, or even asphyxia.

In an attempt to limit the inhalation by the smoker of these three gasesthat are deemed harmful, various types of cigarette filters have beendeveloped, notably filter compositions comprising catalysts in the formof nanometre-size metallic particles (WO 2004/110186) attached to thesurface of porous structures such as zeolites, active carbon or silicabeads. These porous structures can offer a large area of contact withthese gases, so that in the presence of the catalysts, the gases areconverted to carbon dioxide (CO₂) by oxidation. Accordingly, the porousstructures or silica gels are treated with a solution of catalystsbefore they are incorporated in the cigarette filters.

The existing filters of this type therefore have the aim of removingcarbon monoxide, nitrogen oxides and hydrogen cyanide, which areregarded as harmful, by converting them to CO₂ by oxidation. In fact,CO₂ is regarded in the literature as a gas that has no known effect onsmokers' health.

However, as a result of experiments conducted on mice, and describedbelow, the present inventors demonstrated, surprisingly, that CO₂induces an inflammatory reaction in the lungs. In fact they found a verysignificant increase in expression of the proteins β-catenin andNF-κBp65, in the lung tissues of mice that had inhaled air with a CO₂content above 10% (without a decrease in the proportion of oxygen). Thisincrease, which reflects an inflammatory state of the pulmonary cells,was not found in mice inhaling atmospheric air, i.e. air containing lessthan 2% CO₂ (Example 1 presented below). The inventors also showed thatthe inflammation found in the mice could be eliminated partially or evencompletely by selectively trapping the CO₂ contained in tobacco smoke bymeans of a filter that includes a solution of potassium hydroxide (KOH)(Example 2 presented below).

It therefore appears that, contrary to what has been assumed to date inthe literature, CO₂ released by the combustion of tobacco has asignificant role in inflammation of the epithelial tissues of therespiratory tract, such as those of the throat and of the lungs.

Moreover, since cancers of the respiratory tract, such as those of thethroat and of the lungs, are correlated with the number of cigarettessmoked, as well as with the number of years during which an individualis exposed to tobacco smoke, it is assumed that inflammation of thetissues precedes the appearance of tumours in a great many cancer cases[Schwartz L. et al. Cancer: the role of extracellular disease. MedHypotheses. (2002) 58(4):340-61]. Thus, inflammation of the respiratorytract associated with CO₂ is regarded by the inventors, owing to itswide occurrence, as a phenomenon with a determining role in theinitiation of tobacco-linked cancers, equally, or even more, than thepresence of the numerous carcinogenic substances contained in tobaccosmoke.

Medically, moreover, it is recognized that chronic inflammation oftissues promotes the appearance of pulmonary fibroses and thedevelopment of cancers.

In the blood vessels, the inflammatory mechanisms are very similar tothose responsible for the inflammation observed in the pulmonary alveoliin response to cigarette smoke. Furthermore, the inflammatory responseto cigarette smoke (notably secretion of interleukin-6 and TNF-alpha,recruitment of leukocytes) demonstrated by the inventors is also a majorfactor in the development of atherosclerosis, as well as cardiovascularevents.

Thus, CO₂-related inflammation of the arteries is regarded by theinventors, in view of its frequency, as a phenomenon with a determiningrole in the initiation of tobacco-related cardiovascular events,equally, or even more, than the presence of the numerous toxicsubstances contained in tobacco smoke.

It is in fact medically recognized that chronic inflammation of thevessel wall promotes the appearance of atheromatous plaques and thedevelopment of cardiovascular diseases.

In order to overcome these risks, the inventors propose, via the presentapplication, incorporating in air filters, and notably cigarettefilters, means for reducing the proportion of CO₂ resulting from thecombustion of tobacco. These means can be implemented in large filters,such as those for ventilating public places, or in smaller filters, suchas cigarette filters.

The invention relates more particularly to fixed or detachable cigarettefilters that can contain such means.

“Fixed filter” means a disposable filter such as those that are insertedin the end of cigarettes by the manufacturer during their manufacture.

“Detachable filter” means a filter that can be used several times andwhich, according to a preferred aspect, can be cleaned or regenerated.

FIG. 1 presents a graph in which the ordinate shows the Penh indexmeasured by plethysmography on Balb c/ mice used in the experimentdescribed in Example 1, and the abscissa shows the successive injectionsof CO₂ (5, 10 and 15%) carried out every two minutes in the air inhaledby said mice.

FIG. 2 shows two diagrams. These diagrams compare the relativeconcentration of the protein p-catenin and of the protein NF-κB p65 incellular extracts from the lungs of mice sacrificed after inhalation ofair containing 15% CO₂ for 10 minutes and of control mice that inhaledatmospheric air.

FIG. 3 presents four graphs showing, as a function of time, theconcentrations of CO₂ or of O₂ in mmHg measured in the chambers in whichthe experiments described in Example 2 were carried out. The respectiveconcentrations of CO₂ and of O₂ are measured at the outlet from thecigarette in graphs 3A and 3C, and at the outlet from the filtrationcolumn in graphs 3B and 3D. The measurements were performed in foursituations: ♦(control/H₂O): control air filtered by the columncontaining water, ▪(control/KOH): control air filtered by the columncontaining potassium hydroxide, ▴(smoke/H₂O): cigarette smoke filteredby the column containing water, X (smoke/KOH): cigarette smoke filteredby the column containing potassium hydroxide.

FIG. 4 presents a diagram showing the number of cells producing theprotein RANTES (SFC for Spot Forming Cells, ELISPOT technique) in a wellcontaining 2×10⁵ pulmonary cells from mice sacrificed after inhalationof air or cigarette smoke for 38 minutes. The four situations summarizedin the commentary of the aforementioned FIG. 3 are shown.

FIG. 5 presents a diagram showing the number of cells producing theprotein IL-6 (SFC for Spot Forming Cells, ELISPOT technique) in a wellcontaining 2×10⁵ pulmonary cells from mice sacrificed after inhalationof air or cigarette smoke for 38 minutes. The four situations summarizedin the aforementioned commentary of FIG. 3 are shown.

FIG. 6 presents a diagram showing the concentration of chemokine MIP-2(ELISA technique), in the medium after 20-hour culture of cells isolatedfrom the lungs of mice sacrificed after inhalation of air or cigarettesmoke for 38 minutes. The four situations summarized above in thecommentary of FIG. 3 are shown.

FIG. 7 presents a diagram showing the concentration of TNF-alpha (ELISAtechnique), in the medium after 20-hour culture of cells isolated fromthe lungs of mice sacrificed after inhalation of air or cigarette smokefor 38 minutes. The four situations summarized above in the commentaryof FIG. 3 are shown.

FIG. 8 presents a diagram showing the activity of the proteins NF-κB p65in cellular extracts from the lungs of mice sacrificed after inhalationof air or cigarette smoke for 38 minutes. The four situations summarizedabove in the commentary of FIG. 3 are shown.

FIG. 9 presents a diagram showing the activity of phosphatase PP2A incellular extracts from the lungs of mice sacrificed after inhalation ofair or cigarette smoke for 38 minutes. The four situations summarizedabove in the commentary of FIG. 3 are shown.

The present invention therefore relates to the use of means for trappingCO₂ in a cigarette filter to reduce the proportion of CO₂ inhaled by asmoker resulting from the combustion of tobacco.

It relates more particularly to the use of one or more of these meansfor trapping CO₂ for the preparation of a filter intended for preventingcancer or inflammation and/or cardiovascular diseases in a subjectexposed to tobacco smoke.

“Trapping” means any means for immobilizing CO₂ on a molecular supportor its conversion to another chemical entity.

Preferably, said means make it possible to trap at least 20% of the CO₂that would be inhaled by the smoker, more preferably at least 40% andeven more preferably at least 60% of the CO₂ that would be inhaled bythe smoker. The amounts of CO₂ trapped are expressed here relative tothe amount of CO₂ present in the gas phase resulting from the combustionof tobacco.

The amount of CO₂ trapped is expressed here as a percentage of the(molar) amount of CO₂ relative to the total amount of CO₂ present in thegas phase resulting from the combustion of tobacco, in its main, primarystream, in a cigarette without filter. This calculation results fromcomparison of measurements taken by means of an analyticalcigarette-smoking machine in the presence and in the absence of themeans for trapping CO₂ incorporated in the cigarette or in the filter,according to a standard method that complies with current specifications(The standardized conditions are defined in Standard 3308 of theInternational Standards Organization (ISO) with the title: “Routineanalytical cigarette-smoking machine”).

The means envisaged according to the invention are preferably means foradsorption of CO₂.

They make it possible to reduce or limit the proportion of CO₂ thatwould be inhaled by the smoker.

These means, as such, are known by a person skilled in the art and havebeen used in fields of application unrelated to cigarette filters.

The means of the invention can be combined with other filtering means tolimit the emission of particles or of toxic gases other than CO₂.

These means, as well as the structure of the cigarette filters are wellknown by a person skilled in the art [Davis D. L. and Nielsen M. T. eds.(1999) Tobacco: Production, Chemistry and Technology, BlackwellScience].

Another subject of the invention is a filter composition comprising atrapping means as defined above for preventing inflammation and/orcancer and/or cardiovascular diseases in a subject exposed to tobaccosmoke.

“Filter composition” means any mixture of solid and liquid materialshaving the effect of forming a filter, i.e. a structure capable ofretaining solid particles and/or of trapping molecules in gaseous form,such as CO₂.

A preferred means for trapping CO₂ is a means for adsorption of CO₂.

A means for adsorption of CO₂ that is preferred according to theinvention is active carbon. Active carbon can be manufactured forexample from carbonized coconut shells. This material produces a carbonwith a strong granular structure, reducing the formation of dust. It is“activated” by treatment with superheated steam at 800-1000° C., whichhas the effect of very significantly increasing the porosity of thecarbon, thus giving a specific surface between 500 and 3500 m²/g,generally between 500 and 1500 m²/g.

An active carbon according to the invention is for example that marketedby Sud Chemie (Lenbachplatz 6, 80333 Munich, Germany) which is able toadsorb about 4 mol of CO₂ per kg of active carbon at 22° C., 250 psi inthe presence of 15% CO₂, 82% N₂ and 3% O₂ and H₂O, 19 cc/min, or theactive carbon sold under the trademark MAXSORB® by Kansai Coke ChemicalsCo. Ltd. [Otowa, T. et al. Production and adsorption characteristics ofMAXSORB: high-surface-area active carbon.(1993) Active carbon and carbonmolecular sieves 7(4):241-245].

A filter composition according to the invention preferably comprises acigarette filter.

A cigarette filter according to the invention generally contains between0.1 and 3 g and preferably between 0.2 and 2 g of an active carbonaccording to the invention.

Another preferred means of adsorption of CO₂ according to the inventioncomprises the use of zeolites. The zeolites are hydratedaluminosilicates, of natural origin (volcanic rock) or synthetic origin.Their chemical structure is a complex crystal lattice, having numerouscavities containing water molecules and positively-charged ions (notablyK⁺ and Ca²⁺).

Once the water has been removed by heating, the cavities can be occupiedby chemical compounds depending on the size of the molecules and theirpolarity, such as molecules of CO₂.

Zeolites that are preferred according to the invention arehigh-aluminium zeolites, i.e. for which the silicon/aluminium ratio inthe crystal is between 1 and 5, preferably between 2 and 5, and morepreferably between 3 and 5.

The high-sodium zeolites are also preferred. These types of zeoliteshave in fact shown a higher capacity for adsorption of CO₂.

The zeolites, for example those of type 4A and 5A, i.e. zeolitesgenerally having pores between 0.3 nm and 0.8 nm, preferably between 0.4and 0.7 nm and more preferably between 0.5 and 0.7 nm are particularlysuitable, as well as those with a crystal structure of type X, i.e.hexagonal, such as zeolites 13X.

The company Zeochem AG markets a zeolite 13X that is particularly usefulfor this purpose, which is capable of adsorbing about 6-7 mol of CO₂ perkg of zeolite 13X at 22° C., 250 psi, in the presence of 15% CO₂, 82% N₂and 3% O₂ and H₂O, 19 cc/min. Another type of zeolite that can be usedfor the adsorption of CO₂ is Siliporite®, marketed by the company CECA,used notably in an oxygen concentrator, the MEDOX (Medical OxygenConcentrator).

A cigarette filter that is preferred according to the inventiongenerally contains between 0.1 and 3 g, preferably between 0.2 and 2 gof a zeolite according to the invention. According to a preferred aspectof the invention the zeolites can be treated beforehand with polarsolutions, for example solutions of an amine or ether compound, in orderto increase their adsorption capacity as stated in U.S. Pat. No.6,908,497.

A means for adsorption of CO₂ that is preferred according to theinvention comprises the use of MOFs (Metal-Organic Frameworks). The MOFsare crystalline materials of low density constituted of units of zincand of oxygen joined together by organic molecules such as1,4-benzenedicarboxylate [Yaghi, O., Science, 295:469]. Their crystalstructure is such that gas molecules can even be stored inside thecrystal lattice. MOFs are easily synthesized and certain adaptations tothe composition of the organic chains are possible so that the crystalstructure is provided with chemical groups that allow interactions withthe gas molecules that are to be adsorbed. It is also possible to alterthe size of the crystal by modifying the organic chains to provide anoptimum size for the adsorption of CO₂ molecules. According to theinvention, the MOF used is more particularly selected from thefollowing: MOF-177, IRMOF-1, IRMOF-6, IRMOF-3, IRMOF-11, Cu₃(BTC)₂,MOF-74 and MOF-505 [Millward A. R. et al. (2005) Metal-organicframeworks with exceptionally High Capacity for storage of carbondioxide at room temperature, J. Am. Chem. Soc., 127:17998-999].

A cigarette filter that is preferred according to the inventiongenerally contains between 0.1 and 3 g, preferably between 0.2 and 2 gof MOF.

The various means described above that can be used according to theinvention for trapping and more particularly for adsorbing CO₂ aregenerally incorporated in cellulose acetate filters in the form of atransverse segment a few millimetres thick to provide maximum trappingof the gas stream inhaled by the smoker. Alternatively, these means canbe dispersed uniformly in the filter or according to a concentrationgradient in the same direction as this stream or in the oppositedirection.

A cigarette filter according to the invention more generally comprisesmeans for adsorption of CO₂ that can trap at least 20%, preferably atleast 40% and more preferably at least 60% of the proportion of CO₂resulting from the combustion of tobacco inhaled by a smoker.

The invention also relates to a cigarette comprising a filter as definedpreviously.

The invention also relates to a method of filtering cigarette smoke,characterized in that it includes a stage comprising selective trappingof the CO₂ resulting from the combustion of tobacco by means of a filtercomposition according to the invention, notably before the gases arisingfrom said combustion are inhaled by the smoker.

In said method, the CO₂ can be trapped by a means for adsorption of CO₂as defined previously.

The use of a means for trapping CO₂ in a filter or a cigarette, asdefined previously, aims more particularly to limit the risks ofinflammation, of cancer and/or of cardiovascular diseases of a subjectexposed to tobacco smoke, and more particularly inflammation and cancerof the respiratory tract, in particular of the lungs or of the throat.

With regard to cardiovascular diseases, the invention aims moreparticularly to prevent atherosclerosis and its consequences.

The present invention thus relates to a method of preventinginflammation, cancer, and/or cardiovascular diseases, characterized inthat it restricts the proportion of CO₂ inhaled by a subject, moreparticularly by a smoker. This method aims more particularly to preventcancer or inflammation of the respiratory tract, as well ascardiovascular diseases in a subject exposed to tobacco smoke. Moreparticularly said method uses one or more of the means of trapping CO₂as defined previously for the preparation of a filter or of a filtercomposition according to the invention.

The examples given below are for the purpose of illustrating theprinciples of the invention without limiting the scope of protectionrequested.

EXAMPLE 1 Demonstration of an Inflammatory Effect of CO₂ on thePulmonary Cells

1/ BALB/c mice were placed in a closed chamber in which the proportionof CO₂, at constant proportion of oxygen, was raised artificially to 2(atmospheric air control), 5, 10 and 15% by injection of CO₂ into thechamber every other minute. At each of these concentrations,non-invasive functional testing was carried out on the mice byplethysmography, according to the technique described by Hamelmann etal. (1997) Am J Respir Crit Care Med 156: 766-775). This techniqueinvolves assessing the respiratory distress of the mice by determiningthe Penh (enhanced pause) value. The Penh value is a parameter thatnotably makes it possible to measure the ratio of the expiratory andinspiratory amplitude and thus evaluate the extent of asthma attacks,i.e. the inflammatory state of the bronchi and bronchioles owing to areduction in diameter of the latter (respiratory resistance).

The results obtained are presented in the graph in FIG. 1. It followsfrom this experiment that the Penh value increases when the proportionof CO₂ increases. This value is doubled when the proportion of CO₂changes from 10 to 15%, reaching a level that is 6 times higher than thecontrol. Thus, a mean proportion of CO₂ of 13%, equivalent to thatresulting from the combustion of tobacco, has a considerable effect onthe respiratory system, causing inflammation.

2/After keeping the mice for 10 minutes in the chambers at the variousconcentrations of CO₂ stated above, the mice were sacrificed (one hourafter the start of the experiment) in order to determine the proteinsβ-catenin and NF-κBp65 in the nucleus of their pulmonary cells.

The protein β-catenin is a transcription factor that acts on the cellcycle, and is implicated notably in cellular proliferation and in lungcancer [Lim J. H. (2006) Cancer Res; 66(22): 10677-82].

The protein NF-κBp65 is a transcription factor in the NF-κBfamily,contributing to the activation of a great many oncogenes and genesimplicated in the inflammatory response [Nishikori, M. (2005) J. Clin.Exp. Hemathopathol. 45(1):15-18].

These two proteins are recognized markers of inflammation and of cancer.They were determined on the basis of optical density using specializedkits. β-Catenin was determined by ELISA (Catenin Enzyme Immunoassay Kit,Assay designs, Ann Arbor, Mich.) following the manufacturer'sinstructions. The protein NF-κB p65 was determined by another ELISAassay (TrasAM NF-κB p65 nuclear DNA based ELISA, Active Motif,Rixensart, Belgium) following the manufacturer's instructions. Thevalues obtained, presented in the diagram in FIG. 2, are expressedrelative to the total amount of proteins extracted from the cellnucleus.

The increase in the concentration of the proteins β-catenin and NF-κBp65 in the nucleus reflects a state of inflammation or of deregulationof the cells, which is directly attributable to the increase in CO₂concentration.

EXAMPLE 2 Demonstration of an Inflammatory Response in Mice SpecificallyLinked to the CO₂ Contained in Cigarette Smoke

The following experiment involved causing mice to inhale cigarette smokein which most of the CO₂ had been trapped selectively. The CO₂ wastrapped selectively by reaction with a solution of potassium hydroxide(CO₂+H₂O⇄H₂CO₃; H₂CO₃+2KOH⇄K₂CO₂+2H₂O). A solution of water serves asnegative control. For this, cigarette smoke was brought into contactwith the water or the potassium hydroxide by passing through afiltration column containing these solutions.

The set-up employed for the experiment comprises: a suction pumpspecially adapted for consuming cigarettes. The smoke thus obtained issent to a 250-ml sealed chamber, which is connected to a second chamberwith a capacity of 1600 ml via a column which is half-filled with a 1MKOH solution or with distilled water at pH=7. A pair of sensors fortaking measurements of the concentration of O₂ and of CO₂ are arrangedinside each chamber. The measurements were taken every minute for 38minutes, and the results obtained are shown in FIG. 3. The KOH solutionensures a considerable decrease in the concentration of CO₂ present incigarette smoke, which decreases by 50 to 70% (see FIG. 3) withoutsignificantly altering the concentration of oxygen.

The experiment was conducted on BALB/c mice aged from 6 to 7 weeks underin vivo conditions. The number of mice used was 32 males, divided intofour groups of eight. The mice were placed in the second chamber of theset-up (1600-ml chamber) and they breathed either air (control group) orcigarette smoke that had passed through the connecting column betweenthe two chambers containing either distilled water or a 1M KOH solution.Each experiment lasted 38 minutes, or typically the equivalent of theconsumption of 5 cigarettes by a smoker.

The mice were sacrificed after inhalation of air for 38 minutes in thefour situations described above (see also the commentary of FIG. 3) andthe lungs were removed immediately for analysis.

The lungs were analysed in order to measure the activity or thesecretion of six proteins that are known markers of inflammation. Someof these proteins are also known to be markers of certain cancers andatherosclerosis (NE-κB, PP2A). These proteins are as follows: RANTES,IL-6, TNF-alpha, MIP-2, PP2A and NE-κB p65. The three first proteinsbelong to the cytokine family. MIP-2 is a chemokine secreted bymacrophages which permits recruitment of neutrophils. PP2A is aphosphatase known for its role in the induction of apoptosis byinhibition or activation of the pro- or anti-apoptotic pathways.Deregulation of its activity is linked to cancers, in particular lungcancer [Van Hoof C. and Goris J. PP2A fulfills its promises as tumoursuppressor: which subunits are important? (2004) Cancer Cell5(2)105-61]. Finally, NF-κB p65 is a transcription factor, which playsan important role in the activation of genes of proteins involved ininflammatory reactions, for example TNF-alpha. This protein is notablyimplicated in atherosclerosis [Valen G. et al. Nuclear factor kappa-Band the heart. (2001) J. Am. Coll. Cardiol. 38(2):307-14]. Measurementsof activity or of relative concentration of these proteins wereperformed using the following commercial kits: Mouse TNF-alpha/TNFSF1ADuoSet (ELISA assay for the concentration of TNF-alpha); MouseCXCL2/MIP-2 DuoSet (ELISA assay for the concentration of MIP-2), MouseCCL5/RANTES ELISpot Kit (ELISpot assay for the secretion of RANTES);Mouse IL-6 ELISpot Kit (ELISpot assay for the secretion of IL-6), allfrom R&D Systems (Minneapolis, Minn., USA).

The results obtained are presented in FIGS. 4 to 9. These results showthat when the concentration of CO₂ in cigarette smoke is reduced, theinflammation of pulmonary cells is less, based on the markers that wereanalysed. Accordingly, tobacco smoke would be less irritant and likelyto cause cancers of the respiratory tract and cardiovascular diseases ifa significant proportion of the CO₂ present in tobacco smoke were to beremoved.

1. A filter composition comprising: a CO₂ for preventing inflammation,cancer or cardiovascular diseases in a subject exposed to tobacco smoke.2. The filter composition according to claim 1, wherein the CO₂ trapremoves an effective amount of CO₂ to prevent inflammation of therespiratory tract.
 3. The filter composition according to claim 1,wherein the CO₂ trap removes an effective amount of CO₂ to preventcancer of the respiratory tract.
 4. The filter composition according toclaim 1, wherein the CO, trap removes an effective amount of CO₂ toprevent for preventing atherosclerosis.
 5. The filter compositionaccording to claim 3, wherein the cancer of the respiratory tract islung cancer or throat cancer.
 6. The filter composition according toclaim 1, wherein the CO₂ trap comprises a CO₂ adsorbent.
 7. The filtercomposition according to claim 6, wherein the CO₂ adsorbent is activecarbon, a zeolite or a MOF.
 8. The filter composition according to claim7, wherein the zeolite is of type 4A, 5A or 13X.
 9. The filtercomposition according to claim 1, wherein the filter compositionreduces, proportion of CO₂ inhaled by a smoker resulting from thecombustion of tobacco by at least 20%.
 10. The filter compositionaccording to claim 1, wherein the filter composition is in a cigarettefilter.
 11. A method of trapping CO₂ contained in tobacco smoke,comprising: incorporating a CO₂ adsorbent into a filter so as to reduceinflammation, cancer or cardiovascular diseases in a subject exposed totobacco smoke.
 12. A method according to claim 11, wherein the filter isintended to prevent inflammation of the respiratory tract.
 13. A methodaccording to claim 11, wherein the CO₂ adsorbent is an active carbon, azeolite or a MOF.
 14. A method of preventing inflammation, cancer and/orcardiovascular diseases in a subject exposed to tobacco smoke,comprising: trapping the CO₂ resulting from the combustion of tobacco.15. The filter composition according to claim 1, wherein the filtercomposition reduces the proportion of CO₂ inhaled by a smoker resultingfrom the combustion of tobacco by at least 40%.
 16. The filtercomposition according to claim 1, wherein the filter composition reducesthe proportion of CO₂ inhaled by a smoker resulting from the combustionof tobacco by at least 60%.